Protective effect of L-ascorbic acid against oxidative damage in the liver of rats with water-immersion restraint stress

Yashiro

Ohashi

et al. 2015

J Nutr Sci Vitaminol

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Water-immersion restraint stress (WIRS), which is characterized with both psychological stress and physical stress, is widely used to induce reproducible stress ulcers in experimental animals (1). Reactive oxygen species (ROS) and nitric oxide ( • NO) generation, lipid peroxidation, and neutrophil infiltration in the gastric mucosal tissue play a critical role in the pathogenesis of WIRS-induced gastric mucosal lesions (2-5). Iwai et al. (6) have reported that, in rats with 6 h of WIRS, the level of liver lipid peroxide (LPO), which is generated via ROS, increases with concomitant increases in the levels of serum LPO and liver cell damage markers such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities and that pre-administration of gamazumi fruit juice or (2)-epigallocatechin gallate, each of which possesses antioxidant activity, for 2 wk attenuates all these stress-induced changes. Furthermore, the same authors have reported that not only an increase in LPO level but also decreases in superoxide dismutase (SOD) activity and reduced glutathione (GSH) level occur without changes in catalase and glutathione peroxidase activities in the liver of rats with 6 h of WIRS and that preadministration of gamazumi crude extract possessing antioxidant activity to rats with 6 h of WIRS for 2 wk attenuates the increased LPO level and the decreased SOD activity and GSH level in the liver (7). We have reported that, in the liver of rats exposed to WIRS over a 6-h period, cell damage occurs before the appearance of oxidative stress with disruption of antioxidant defense systems associated with decreased ascorbic acid (vitamin C) and GSH levels and SOD activity and enhanced lipid peroxidation, enhanced • NO generation, and neutrophil infiltration in the tissue, although the vitamin E level does not change in the liver tissue (8). We have also shown that a single pre-administration of l-ascorbic acid protects against oxidative damage in the liver of rats with 6 h of WIRS by attenuating disrupted antioxidant defense systems and enhanced lipid peroxidation, enhanced• NO generation, and neutrophil infiltration in Asaminami-ku, Hiroshima 731-0153, Japan (Received October 20, 2014) Summary We examined how dietary supplementation of vitamin E protects against liver oxidative damage in rats with water-immersion restraint stress (WIRS). Before WIRS exposure, rats received a normal diet (ND) or vitamin E-supplemented diet (VESD) (500 IU a-tocopherol/kg diet) at a mean dose of 15 g/animal/d for 4 wk. The two diet groups had serum transaminases and lactate dehydrogenase activities and adrenocorticotropic hormone, corticosterone, and glucose levels to a similar extent. VESD-fed rats had higher liver a-tocopherol concentrations and lower liver ascorbic acid, total coenzyme Q9 (CoQ9), reduced CoQ9, reduced CoQ10, and lipid peroxide (LPO) concentrations than ND-fed rats. When the two diet groups were exposed to 6 h of WIRS, the serum liver cell damage index enzyme activities incr...

Section: Discussionsupporting

confidence: 72%

Section: Discussionsupporting

confidence: 61%

Section: Discussionsupporting

confidence: 58%

Section: Effect Of Dietary Vitamin E Supplementation On Liver Oxidatimentioning

confidence: 99%

Section: Effect Of Dietary Vitamin E Supplementation On Liver Oxidatimentioning

confidence: 99%

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Effect of Dietary Vitamin E Supplementation on Liver Oxidative Damage in Rats with Water-Immersion Restraint Stress

Yashiro

Ohashi

et al. 2015

J Nutr Sci Vitaminol

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Water‐immersion restraint stress disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats

Cell Biochemistry & Function

Yashiro

Kaida

et al. 2012

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We examined whether water-immersion restraint stress (WIRS) disrupts nonenzymatic antioxidant defense systems through ascorbic acid depletion in the adrenal gland of rats. Rats were exposed to WIRS for 0.5, 1.5, 3 or 6 h. WIRS increased serum adrenocorticotropic hormone, corticosterone and glucose concentrations and adrenal corticosterone content at each time point. WIRS increased adrenal lipid peroxide content at 3 and 6 h, and the increase was twofold higher than the unstressed level at 6 h. WIRS decreased adrenal ascorbic acid content at each time point, and the decrease reached one-third of the unstressed level at 6 h. WIRS increased adrenal reduced glutathione content at 0.5 and 6 h but reduced that content to half of the unstressed level at 6 h. WIRS increased adrenal α-tocopherol content at 1.5 h but returned that content to the unstressed level thereafter. When rats with 6 h of WIRS was orally preadministered with l-ascorbic acid (250 mg/kg), WIRS-induced changes in adrenal lipid peroxide, ascorbic acid and reduced glutathione contents were attenuated without any change in stress response. These results indicate that WIRS disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats.

Protective Effect of Brazilian Propolis Against Hepatic Oxidative Damage in Rats with Water‐immersion Restraint Stress

Nakamura¹,

Ohashi

et al. 2012

Phytotherapy Research

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In the present study we examined the protective effect of Brazilian propolis against hepatic oxidative damage in rats with water-immersion restraint stress (WIRS) in comparison with that of vitamin E (VE). Fasted rats orally received Brazilian green propolis ethanol extract (BPEE; 10, 50 or 100 mg/kg), VE (250 mg/kg) or vehicle at 30 min before the onset of WIRS. Exposure of vehicle-treated rats to 6 h of WIRS caused liver cell damage, judging from the levels of serum alanine aminotransferase and aspartate aminotransferease, increased hepatic lipid peroxide, NO(x) contents and myeloperoxidase activity, and decreased hepatic non-protein SH, ascorbic acid contents and superoxide dismutase activity. Preadministration of BPEE (50 or 100 mg/kg) or VE to the stressed rats protected against the hepatic damage and attenuated the increased hepatic lipid peroxide and NO(x) contents and myeloperoxidase activity and the decreased hepatic non-protein SH and ascorbic acid contents and superoxide dismutase activity. These protective effects of BPEE (50 mg/kg) were greater than those of BPEE (100 mg/kg) and were almost equal to those of VE. These results indicate that BPEE protects against hepatic oxidative damage in rats exposed to WIRS possibly through its antioxidant and antiinflammatory properties such as VE.